This session reviewed the impact of epigenetic regulation of gene transcription by chromatin remodelling factors (mainly non-coding RNA-based mechanisms, histone modifications and DNA-methylation) on the cardiovascular system and provides insights as to the factors that may influence the epigenome.

First, Jean Louis Gueant reported on how nutrition (e.g., vitamin B, diet enriched in methyl donors) influence the epigenetic mechanisms for gene expression and emphasized the effect of maternal nutrition on the fetal epigenome and its impact on post-natal health.

The impact of different epigenetic writers and erasers (enzymes that alter histones and/or DNA by adding or removing chemical groups, respectively) on cardiac hypertrophy was further examined by Cinzia Perrino, who provided experimental data that shed light on the mechanisms involved.

Gerald W Dorn II provided data to support that long non-coding RNA (lncRNA) are tissue-specific by analyzing heart, liver and skin. Further assessment of lncRNA by heat maps profiling demonstrated that lncRNA-based epigenetic regulation is greater during embryo-adult transition than during reactive hypertrophy. In this regard, Prof. Dorn outlined the involvement of lncRNA in cardiovascular lineage commitment.

In the last talk, Roger Foo presented the genomic response (either protective and/or deleterious) triggered by heart failure and stressed the differential DNA methylation pattern in end-stage human cardiomyopathic hearts as compared to healthy hearts. Dr. Foo pointed out that such different profiling correlated to changes in specific gene expression. Finally, Prof. R. Foo presented transcriptomic analysis that demonstrate that single cell transcriptome signature differ among cells despite being from the same type.

In summary, the following session provided a comprehensive overview of the available experimental and clinical data on the impact of epigenetics in heart failure and how environmental factors (nutrition) modulates the epigenetic pattern already in early-life playing a role in cardiovascular risk.